Abstract
The effects of the calcium (slow) channel blocker verapamil, on non-cardiac excitable membranes were examined in vivo. In barbiturate anaesthetized cats, the effect of intravenously administered verapamil (0.1, 0.2, and 0.4 mg*kg-1) on isometric twitch amplitude of the flexor carpi radialis muscle, elicited by indirect and direct electrical stimulation, was determined. At all doses tested, verapamil significantly reduced muscle twitch amplitude from control values. The effect of dosage on twitch reduction was far more pronounced for indirect than direct stimulation. Full recovery to control was observed by 90 minutes only with the lowest dose (0.1 mg*kg-1IV). Reduction of twitch amplitude (direct and indirect) lasted the duration of the experiment (180 minutes) for the two higher doses of verapamil. No significant changes in blood pressure, cardiac rate or rhythm were observed. The specific site and mechanism of verapamil’s neuromuscular blocking action remains unclear. In clinical situations where potent inhalation agents, adjuncts or neuromuscular blocking agents may be used, therapeutic doses of verapamil may interact to promote muscle weakness.
Résumé
On a observé les effets du vérapamil, un agent bloquant de calcium (voie lente) sur des membranes non cardiaques in vivo, Chez des chats anesthésiés avec du barbiturate, on a vérifié les effets du vérapamil administré par voie intraveineuse (0.1, 0.2 et 0.4 mg*kg-1) sur la phase isométrique de la contraction du muscle grand palmaire provoqué par stimulation électrique directe et indirecte. A toutes les doses vérifiées, le vérapamil réduisit significativement l’amplitude des contractions musculaires par rapport aux valeurs de contrôle. L’effet du dosage sur la réduction de contractions était beaucoup plus prononcé avec la stimulation indirecte que directe. La récupération au niveau du contrôle a été observée après 90 minutes seulement avec la dose la plus basse (0.1 mg*kg-1 I.V.). La réduction de contractions (directe ou indirecte) dura tout le temps de l’expérience (180 minutes) pour les deux doses plus élevées de vérapamil. On n’observa pas de changements significatifs de pression artérielle, de rhythme ni de débit cardiaque. L’endroit spécifique et le mécanisme d’action du vérapamil comme agent bloquant neuromusculaire ne sont pas éclaircis. En situation clinique où des agents actifs d’inhalation, des traitements d’appoint et des agents bloquants neuromusculaires sont administrés, des doses thérapeutiques de vérapamil peuvent interagir afin d’activer la faiblesse des muscles.
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Supported in part by a Biomedical Research Support Grant from the Texas Tech University Health Sciences Center.
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Kraynack, B.J., Lawson, N.W. & Gintautas, J. Neuromuscular blocking action of verapamil in cats. Can Anaesth Soc J 30, 242–247 (1983). https://doi.org/10.1007/BF03013802
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DOI: https://doi.org/10.1007/BF03013802